Primate cortical area MT plays a central role in visual motion perception, but models of this area have largely overlooked the binocular integration of motion signals. Recent electrophysiological studies tested binocular integration in MT and found surprisingly that MT neurons lose their hallmark "pattern motion" selectivity when stimuli are presented dichoptically and that many neurons are selective for motion-in-depth (MID). By unifying these novel observations with insights from monocular, frontoparallel motion studies concurrently in a binocular MT motion model, we generated clear, testable predictions about the circuitry and mechanisms underlying visual motion processing. We built binocular models in which signals from left-and right-eye streams could be integrated at various stages from V1 to MT, attempting to create the simplest plausible circuits that accounted for the physiological range of pattern motion selectivity, that explained changes across this range for dichoptic stimulus presentation, and that spanned the spectrum of MID selectivity observed in MT. Our successful models predict that motion-opponent suppression is the key mechanism to account for the striking loss of pattern motion sensitivity with dichoptic plaids, that opponent suppression precedes binocular integration, and that opponent suppression will be stronger in inputs to pattern cells than to component cells. We also found an unexpected connection between circuits for pattern motion selectivity and MID selectivity, suggesting that these two separately studied phenomena could be related. These results also hold in models that include binocular disparity computations, providing a platform for future exploration of binocular response properties in MT.
.The effect of anesthetic drugs at central synapses can be described quantitatively by developing kinetic models of ligand-gated ion channels. Experiments have shown that the hypnotic propofol and the sedative benzodiazepine midazolam have similar effects on single inhibitory postsynaptic potentials (IPSPs) but very different effects on slow desensitization that are not revealed by examining single responses. Synchronous oscillatory activity in networks of interneurons connected by inhibitory synapses has been implicated in many hippocampal functions, and differences in the kinetics of the GABAergic response observed with anesthetics can affect this activity. Thus we have examined the effect of propofol and midazolam-enhanced IPSPs using mathematical models of self-inhibited one-and two-cell inhibitory networks. A detailed kinetic model of the GABA A channel incorporating receptor desensitization is used at synapses in our models. The most dramatic effect of propofol is the modulation of slow desensitization. This is only revealed when the network is driven at frequencies that are thought to be relevant to cognitive tasks performed in the hippocampus. The level of desensitization at synapses with propofol is significantly reduced compared to control synapses. In contrast, midazolam increases macroscopic desensitization at network synapses by altering receptor affinity without concurrently modifying desensitization rates. These differences in gating between the two drugs are shown to alter network activity in stereotypically different ways. Specifically, propofol dramatically increases the amount of excitatory drive necessary for synchronized behavior relative to control, which is not the case for midazolam. Moreover, the range of parameters for which synchrony occurs is larger for propofol but smaller for midazolam, relative to control. This is an important first step in linking alterations in channel kinetics with behavioral changes.
Viewing static visual scenes for several seconds or longer can induce a wide variety of striking percepts, including negative afterimages, fading, and motion aftereffects. To characterize the neuronal bases of such phenomena and elucidate functional circuitry in the visual system, we recorded responses of neurons in primary visual cortex (V1) of anesthetized macaques during and after the presentation of prolonged static visual stimuli. We found that 72% of cells generated significant after-responses (ARs) that outlasted classical offtransients after the cessation of stimuli, and AR amplitude grew with stimulus duration. After the longest stimuli tested (32 s), the amplitude and the time course of the AR were on average comparable to, and correlated with, those of the maintained response evoked while stimuli were present. These observations generally held regardless of cell class: simple, complex, direction selective (DS) or non-DS. The average decay time constant of the AR for orientation-tuned cells was 0.65 s. This is strikingly shorter than time constants observed in the lateral geniculate nucleus, which were on the order of tens of seconds. Cells in V1 that lacked orientation tuning displayed an intermediate time course, with a mean time constant of 4.3 s. These results are consistent with a multistage model in which cells at successive stages adapt to their inputs with progressively shorter time constants. Our findings suggest that the perceptual phenomena of fading and afterimages are shaped by both cortical and subcortical dynamics and provide a physiological framework for the interpretation of recent and long-standing psychophysical observations.
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